06
Jul
09

The biochemistry of ethanol consumption

Well, this is really about alcohol consumption in general, coupled with, I hope, a decent review of the underlying mechanisms of what happens psychologically and chemically.

I will be covering the biochemistry in several aspects. The metabolism of ethanol is central to this. Some ethanol is produced by bacteria in the gut, so everyone has, at the very least, a low level of ethanol metabolism. Once ethanol is consumed, it then begins being oxidized by an alcohol dehydrogenase. This enzyme converts ethanol into acetaldehyde. Acetaldehyde is a much more directly toxic substance. Acetaldehyde is then converted to acetic acid which is then converted to acetyl-CoA. At each step of this, the substances have physiological effects on the body which I shall briefly discuss.

Ethanol is an allosteric modulator of GABAA. Since GABAA is an inhibitory neurotransmitter receptor, which causes a decrease in neuron firing, GABAA is essentially a depressant receptor. Continuous activation of GABAA results in it being downregulated to allow for the nervous system to function properly. This is what partially causes alcohol tolerance and physical dependence. Complete withdrawal from alcohol after prolonged heavy use can result in uncontrolled synapse firing. (siezure, convulsion, etc.)Some medications can reduce this hypersensitivity of neurons. This is why severe alcoholics generally must undergo “detox” to treat these physiological effects of alcohol dependence prior to a therapy to prevent relapse.

Acetaldehyde is one compound which contributes to hangovers and is partially responsible for the damage associated with alcohol consumption. It has been hypothesized that cirrhosis may partially be due to acetaldehyde. Additionally, prolonged use of alcohol results in fatty deposits in the liver, although the exact mechanism of this is unknown. Acetaldehyde also is a potent carcinogen and mutagen which is partially responsible for many of the cancer and disease risks associated with smoking, car exhaust, and alcohol consumption.

As for the beneficial effects of ethanol consumption in low to moderate levels (less than two drinks per day), there is good evidence that this is the case. These include a decreased incidence of cardiovascular disease and some protection from some infectious diseases and diabetes. In higher levels, however, these benefits seem to be countered by greater than two drinks per day. The optimal point of mortality associated with alcohol is near the one drink per day mark.

As for the physiological effects of alcohol withdrawal, these are slightly more complex. The most severe of the symptoms are anorexia, delirium tremens, diarrhea, hyperthermia, nausea, seizures, sweating, and tachycardia. All of these are due to the overexcited state of neurons. Typically given to suppress these effects are a range of GABA modulators such as benzodiazepines, Carbamazepine, and Flumazenil. These medications are typically given due to the ease which these can be metered.

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16 Responses to “The biochemistry of ethanol consumption”


  1. 2 jaredcormier
    July 6, 2009 at 7:43 pm

    Thanks, I try sometimes. As always, let me know if you find errors or have questions. I’ve read enough about it in the past few days to spew volumes of data at you if a question is asked, so be specific. I also have a case study which I shall not discuss in an open forum

  2. 3 Colloquy
    July 6, 2009 at 7:47 pm

    Do u want me to be a case study? I’m gonna go “consume” right now – what do u want to know?

  3. 4 jaredcormier
    July 6, 2009 at 7:54 pm

    Haha, no I was talking about a long term case study relating to the physiology of addiction, but thanks for the offer. You have fun! Drink one for me, I can’t keep any in the house.

  4. July 18, 2009 at 6:27 am

    I wonder if this means there’s an objective way of measuring alcohol or benzodiazepine tolerance, at least partially. If tolerance can be defined by the prevalence of GABAa receptors, maybe there’s some way we could gauge how “tolerant” a person is. This could be useful if someone gets prescribed benzodiazepines and is already cross-tolerant to alcohol (hence in normal dosages, benzos won’t work on him)

  5. 6 jaredcormier
    July 18, 2009 at 9:16 am

    Without being highly invasive, probably not, although you could look at neuron excitation. If someone does drink enough to have a marked physiological effect, benzodiazepines should be avoided, anyway, as should any GABA receptor activator.

  6. July 18, 2009 at 9:22 am

    In that case, it just might be that there are other indirect markers for tolerance that can be measured. Frankly, I wouldn’t trust a mere MRI of the brain – our brains don’t come out of ACME, and every brain reacts differently. However, marked discrepancies in receptor expression would be a pretty incisive signifier of tolerance.

    I was kinda thinking that, since GABA receptors are unique to the brain, then you would be able to spot their prevalence somehow without directly looking at it.

  7. 8 jaredcormier
    July 18, 2009 at 9:27 am

    Feel free to try some experiments, I just don’t know exactly HOW you could measure it without directly looking at it. Perhaps by somehow decreasing GABA receptor activity then increasing it, you could quantitate the number of receptors, alternatively, you would be able to look at mRNA transcripts of the various GABA receptor subunits, but this would also be rather invasive.

  8. July 18, 2009 at 9:33 am

    My premise is that maybe GABA receptors are expressed (and are thus prevalent at) the blood stream in any given moment – and you can notice the discrepancies in alcoholics with non-alcoholics and moderate drinkers being the control. I don’t have enough medical knowledge to know whether or not this is the case. If such tests were available, though, I think it could save a lot of patients a lot of anguish.

    Think of serotonin, for example. BBB passable, there’s a lot of serotonin in the intestines at any given moment, supposing it was possible to see what is “normal” serotonin prevalence – you could link hyper- or subnormal levels with psychological conditions, without ever looking at the brain.

  9. 10 jaredcormier
    July 18, 2009 at 9:45 am

    Everything I’ve read on measuring the prevalence of GABAa receptors involves homogenates of some kind or lysing neurons. GABA (neurotransmitter) may not even be BBB passable. I’m going to rack my brain and see if I can’t think of any way to test GABAa expression without taking out chunks of nerve tissue….

  10. July 18, 2009 at 10:22 am

    Well, obviously, the easiest way to measure anything in the body would be, erm, an autopsy, but that’s hardly what I meant :=)

  11. 12 jaredcormier
    July 19, 2009 at 1:35 pm

    radiolabeled Flumazenil and PET scans… You can view the distribution and expression level of GABA receptors.

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